An Incomplete Anterolateral Papillary Muscle Rupture in Patient with Suspected Septic Shock

Abstract

Papillary muscle rupture (PMR) is a cardiac surgical emergency, and early treatment is associated with better short- and long-term survival outcomes. The sensitivity of the transthoracic echocardiogram for PMR is rather low (65%), and in acute, the diagnosis could be difficult given the clinical, laboratory, and radiological aspects not specific for the disease. We report a case of incomplete anterolateral PMR in a patient admitted to intensive care with bilateral pneumonia and septic shock. Transesophageal echocardiogram was fundamental for a better visualization of mitral subvalvular apparatus, allowing a correct diagnosis and a tempestive treatment.

INTRODUCTION

Papillary muscle rupture (PMR) is a rare mechanical complication of acute myocardial infarction (AMI) occurring mainly in elderly patients in absence of previous cardiovascular events, associated with a high in-hospital mortality rate.[1] The posteromedial papillary muscle is the most affected muscle due to his single-coronary vascularization instead of the anterolateral, which receives dual vascularization (circumflex and left anterior descending artery).[1] Clinical and radiologic presentation of PMR is not always clear and could mimic a bilateral pneumonia with septic shock.[2]

CASE REPORT

A 70-year-old woman referred to the emergency department for increasing dyspnea. Her personal medical history included chronic obstructive pulmonary disease and arterial hypertension. The patient was conscious, tachycardic, and tachypneic, with marbled skin and no peripheral edema. Cardiac auscultation revealed an irregular rhythm in the absence of murmur. Blood pressure was 90/60 mmHg; heart rate was 110 beats/min. Arterial blood gas showed metabolic acidosis with increased lactates and hypocapnic hypoxia with oxygen flow rate of 12 L/min. Blood tests showed leukocytes, predominantly neutrophils, increased C-reactive protein (CRP), alteration of liver function, and bacteria and leukocytes in urinary sediment [Table 1].

Table 1.

Blood test

Parameters	Values
WBC	13.44×103/L
NEUT	87.2%
HGB	12.4 g/dL
MCV	98
HCT	36.4%
PLT	122×103/L
CRP	8.24 mg/dL
INR	1.3
Albumin	1.94 g/dL
AST	885 U/L
ALT	417 U/L
LDH	462 U/L
CK	87 U/L
Urine pH	6
Leukocyturia	32
Bacteriuria	1143

WBC=White blood cell, NEUT=Neutrophils, HGB=Hemoglobin, MCV=Mean corpuscular hemoglobin, HCT=Hematocrit, PLT=Platelet, CRP=C-reactive protein, AST=Aspartate aminotransferase, ALT=Alanine transaminase, LDH=Lactate dehydrogenase, CK=Creatine kinase

Electrocardiogram was reported as “atrial fibrillation with nonspecific ventricular repolarization abnormalities” [Figure 1].

Figure 1.

Twelve-lead electrocardiogram

In emergency room, suddenly, the patient accused loss of consciousness with hypotension and severe desaturation. The anesthetist proceeded with orotracheal intubation and volume replenishment using balanced crystalloids followed by infusion of noradrenaline. Transthoracic echocardiography (TTE) excluded indirect signs of pulmonary embolism and showed a normal left ventricle (LV) systolic function. Total-body computed tomography confirmed the absence of pulmonary embolism and revealed multiple pulmonary consolidations descripted as bronchopneumonia in the absence of pleural effusion. The patient was transferred to intensive care with the diagnosis of pneumonia and septic shock. Rapidly, the clinical conditions worsened: the patient became anuric and hypotensive despite infusion of vasoconstrictors. A continuous venovenous hemodiafiltration was started. The blood chemistry tests were repeated, showing a progressive worsening of hepatic and renal function and alteration of coagulation parameters. Cardiac biomarkers were added to routine tests, and high-sensitivity cardiac troponin (hs-TnT) resulted in markedly elevated [Table 2].

Table 2.

Blood test in intensive care unit

Parameters	Values
PLT	45.000×103/mm3
INR	2.5
D-dimer	19,804 ng/mL
Creatinine	3.09
AST	5785 U/L
ALT	2187 U/L
LDH	7250 U/L
CK	237 U/L
hs-TnT	60,639 pg/mL
CK-MB	2.5 ng/mL
Mb	375.5 ng/mL

PLT=Platelet, AST=Aspartate aminotransferase, ALT=Alanine transaminase, LDH=Lactate dehydrogenase, CK=Creatine kinase, hs-TnT=High-sensitivity cardiac troponin, CK-MB=Creatine kinase-myocardial band, Mb=Myoglobin

Due to a significant increase in hs-TnT, TTE was repeated and reported: “LV anterolateral and inferolateral mid-distal wall hypokinesia. Severe mitral insufficiency with prolapse of the posterior mitral leaflet presenting isoechoic round formation (bacterial endocarditis?).” To better characterize the mass described, a transesophageal echocardiography (TEE) was performed. In transgastric short-axis view, it was possible to confirm abnormal LV systolic function [Video 1]. Three-chamber view allowed to visualize the mass below the mitral annulus following leaflet movements and with a similar LV-free wall echogenicity [Figure 2 and Video 2]. Off-axis views helped us to define this cardiac mass: an incomplete rupture of anterolateral papillary muscle secondary to ischemia [Figure 3 and Videos 3 and 4]. Three-dimensional TEE reconstructions in surgical view showed how the ruptured papillary muscle prolapse in the atrium during systole, mainly at the P1 and P2 scallops [Figure 4 and Video 5].

Figure 2.

The three-chamber view reveals a mass below the mitral leaflet with similar echogenicity to the ventricle wall

Figure 3.

Off-axis transgastric view shows incomplete rupture of anterolateral papillary muscle

Figure 4.

Three-dimensional transesophageal echocardiography reveals prolapse of both mitral leaflets, mainly at the P1 and P2 scallops

Color Doppler imaging confirmed severe mitral insufficiency and defined the regurgitation jet origin due to two leaflets prolapse with altered coaptation [Video 6]. Given the impossibility of sustaining circulation despite catecholamines, we proceeded to implant a ventricular assist device (Impella). A coronary angiography was performed showing a three-vessel coronary artery disease. In agreement with cardiac surgeons, surgery was postponed considering patient instability. With Impella support, there was a progressive clinical and laboratory improvement (reduction in transaminases, prothrombin international normalized ratio (INR), creatinine, and increase in platelets). After 72 h, cardiac surgery was performed with excision of the ruptured papillary muscle [Figure 5], bioprosthetic mitral valve (MV) replacement, and double aortocoronary bypass.

Figure 5.

Excision of the ruptured papillary muscle

DISCUSSION

Clinical manifestations of PMR include pulmonary edema, hypotension, or cardiogenic shock. The severe mitral regurgitation systolic murmur may not be audible due to the absence of a gradient between the atrium and ventricle for the large regurgitant orifice.[3] The clinical presentation of PMR can be ambiguous. A rare case of PMR secondary to infective endocarditis with systemic embolization is described in literature.[4] The peculiarity of our clinical case, instead, was to simulate bilateral pneumonia with respiratory failure and septic shock in a patient with AMI in absence of any infectious disease.

The sensitivity of TTE is rather low (65%–85%):[5] in acute, in patient with pulmonary edema and hyperdynamic LV, wall motion segmental abnormalities may be less evident; furthermore, only complete PMR has flail mitral leaflet with a mobile mass attached to chordae tendineae prolapsing completely in the left atrium.[6] There are several mechanisms of mitral prolapse secondary to ischemia: in complete PMR, there is a total papillary muscle detachment, and both leaflets are affected. In partial PMR, a portion of tissue keeps the ruptured papillary muscle attached to the main muscular structure. Incomplete rupture occurs with necrosis of one of several strands of papillary muscle; the leaflet keeps its anchoring system due to chordae tendineae of the remaining strands: there is not leaflet flail.[5] In doubtful cases, especially in partial or incomplete PMR, it may be useful a TEE which allows better visualization of the subvalvular apparatus (sensitivity 92%–100%).[5] TEE can also provide additional findings such as the precise identification of the affected MV segments and the intact papillary muscle (PM) head still attached to the LV wall, sometimes misdiagnosed as a thrombus.[7] In this case, the papillary muscle was initially identified as an endocarditic vegetation and only the TEE imaging allowed to make a correct diagnosis.

Furthermore, laboratory data (showing a significant increase in CRP and neutrophilic leukocytosis) were another misleading aspect in addition to clinical presentation and imaging. In literature, high CRP values are well documented in patients with stable coronary artery disease compared to healthy population. These values significantly increase in case of AMI.[8]

Expeditious surgical treatment of PMR offers a good chance of survival, but postoperative mortality or morbidity is very high. MV replacement is the most commonly used surgical technique.[1] The preoperative status is a predictor of postoperative mortality and so, in some cases, is suitable to delay intervention at patient stabilization to improve successful repair.[6] In recent years, percutaneous edge-to-edge MV repair has become an alternative to surgery in patients with symptomatic severe mitral regurgitation with high surgical risk.[9] Unfortunately, not all centers have access to this technique, particularly in emergency conditions.

In conclusion, PMR is a rare complication of AMI associated with a high intrahospital mortality rate. In presence of acute dyspnea and shock, even in the absence of typical chest pain and systolic murmur, it is necessary to rule out a ruptured papillary muscle, which is a clinical and radiological presentation that could mimic a bilateral pneumonia.

Echocardiographic diagnosis may be difficult, and it could be useful as a TEE in doubtful cases, especially in partial or incomplete ruptures, considering that early diagnosis and treatment are associated with better survival outcomes.

In hemodynamically unstable patient, it may be useful to discuss case in a multidisciplinary team to evaluate the possibility of circulatory assist devices as a bridge to surgery.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.